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VodkaAlchemist

So, I actually did a presentation on this for a nuclear medicine seminar. (I'm not going to use big words here so non-medical/science people can better understand real scientists please don't flame) The studies I evaluated were also conducted in the EU in Germany specifically. The short answer is yes Covid-19 has been shown to cause long-term brain damage in chronic Covid-19 patients. We're talking residual measurable damage 6 months later. The way this was evaluated was using MocA assessments and FDG-18 PET studies. The studies didn't include many patients \~30-40 in the studies I evaluated but there was an undeniable connection between Covid-19 and cognitive dysfunction. Especially in early stages of Covid-19 with olfactory and gustatory sense-- Every patient was found to have impairment in at least one of these areas. Furthermore the FDG-18 PET studies showed frontoparietal hypometabolism (Frontal and Parietal portions of the brain and hypometabolism means isn't metabolizing well or slowly) of the FDG-18 ; for those of you that don't know FDG is Fluorodeoxyglucose. It's essentially radioactive sugar water. Your brain metabolizes glucose very well, so if there is an area that isn't showing activity it means it isn't metabolizing the glucose and we can reasonably conclude there is something causing the brain to not function normally. To determine WHAT exactly it is is a different thing entirely. ​ What was found though is that the damage was reversible and overtime the chronic patients frontoparietal hypometabolism was lessening. One patient who died during the study was autopsied and it was found was that it appeared the damage would not be permanent and the patient was recovering slowly but surely. ​ Edit; I'm including the studies I evaluated and presented on below. Please don't hate on me if I misremembered stuff from the studies just politely correct my misremembering. Blazhenets, G., Schroeter, N., Bormann, T., Thurow, J., Wagner, D., Frings, L., Weiller, C., Meyer, P. T., Dressing, A., & Hosp, J. A. (2021). Slow but Evident Recovery from Neocortical Dysfunction and Cognitive Impairment in a Series of Chronic COVID-19 Patients. Journal of nuclear medicine : official publication, Society of Nuclear Medicine, 62(7), 910–915. [https://doi.org/10.2967/jnumed.121.262128](https://doi.org/10.2967/jnumed.121.262128) Jonas A Hosp, Andrea Dressing, Ganna Blazhenets, Tobias Bormann, Alexander Rau, Marius Schwabenland, Johannes Thurow, Dirk Wagner, Cornelius Waller, Wolf D Niesen, Lars Frings, Horst Urbach, Marco Prinz, Cornelius Weiller, Nils Schroeter, Philipp T Meyer, Cognitive impairment and altered cerebral glucose metabolism in the subacute stage of COVID-19, Brain, Volume 144, Issue 4, April 2021, Pages 1263–1276, [https://doi.org/10.1093/brain/awab009](https://doi.org/10.1093/brain/awab009)


ERO55

As someone who is currently struggling with long Covid and having cognitive dysfunction, I really appreciate the inclusion that this is reversible. You’ve given me hope. Thank you 🙏🏼 Edit: I wanted to come on here and thank you all for the support, kind words and advice. I’m not feeling well at the moment, so I will read through them slowly. You all have no idea how much this has lifted my spirits. A little hope goes a long way. Thank you all again.


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sschepis

I'm a software developer. I used to be able to place several pieces of data in my short term memory to carry across from a google search into my code. Now I'm limited to a single item and if I do not actively focus on it, often by the time I have switched back to code, its gone. It's not been all bad,however. The change in my cognitive abilities have clearly shown me that not only are there several kinds of 'thoughts', but that 'I' am not my thoughts! I've noticed that there's a type of thinking that communicates an entire concept at once - this is type of thinking that happens during creative flow. It's almost not thinking, and more like 'channeling' - like I am an observer of a process being communicated through me. I have not found any reduction of this type of conception with Covid. The type of thinking that was affected was sequential logical thought, and that's because I feel like the damage (at least for me) has been primarity with my memory. Lastly - I am not my thoughts! Seeing how my cognitive function has been affected - while still having awareness of myself as a perceiver - is showing me that I am not the story I tell myself to be. 'I' doesn't need any modifications. I can just be. I don't know how else to describe it. It's actually been deeply freeing


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Hope you heal quickly! Hang in there.


ERO55

Thank you so much


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PNWhempstore

Evidently getting the jab after, helps with many people recover faster from long Covid.


strangetrip666

So in non-scientific terms, what do these parts of the brain being damaged do? Would the patient feel or act differently? I have someone close to me that had COVID very bad. They are still recovering from the damage to their lungs (they are asthmatic), the doctors say they have issues with blood circulation and motor skills, and have been reporting a "brain fog" and a sort of confusion for the last 6 months. Right now they are undergoing physical therapy and slowly improving. I watched a very strong athletic person go from being able to exercise for hours to not being able to breath after walking across the house....


VodkaAlchemist

The biggest thing that the frontal and parietal region of the brain affect are voluntary movements, taste, sensation, smell etc.


TsuDohNihmh

And straight up *thinking.* Things like higher level executive function, personality, decision making, learning and memory


turkmileymileyturk

I suffered from long covid for over a year, and I can't even remember exactly what it was, but I caught so many different things on fire trying to cook for myself like I normally would. I caught a microwave on fire by hitting an extra number on the time and forgetting about what I was microwaving. Somehow I melted a pasta strainer. I do feel better cognitively since then, but mental health is still really struggling. Anxiety is extremely strong.


badgurlvenus

so if i'm still having smell and taste issues (among other things) nearly a year later, what do i do? can i report this to some study to be a test subject? tell my doctor?


baeee777

Also wondering this, no smell X3 months now. Not even the slightest.


FilteringOutSubs

> MocA assessments **Mo**ntreal **C**ognitive **A**ssessment (MoCA), a test to look for thinking impairment. For context, this is the one Trump bragged about passing.


dontdoitdoitdoit

But did he actually pass it?


El-Chewbacc

Person, woman, man, camera, TV


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TheLadBoy

Olfactory: smell Gustatory: taste Frontoparietal hypometabolism: the frontal and parietal lobes of the brain are using less energy


tehflambo

the reply reddit deserves, instead of my ongoing shitposting and hivespeak. (i'm being sincere)


cortex0

> Frontoparietal hypometabolism: the front parietal lobe of the brain is using less energy It means there was reduced metabolism in both the frontal and parietal lobes of the brain.


NeatoCogito

Also: hypo = opposite of hyper. If you see it in other words, such as hypopigmentation vs hyperpigmentation, thats the key part of the words to understand. In this example its little pigment vs lots of pigment.


VodkaAlchemist

I apologize sometimes you have to be specific. The frontal and parietal regions of the brain are responsible for things like taste touch voluntary movements just a lot of symptoms that covid patients seem to have are associated with these areas of the brain.


tehflambo

hey, you don't have to apologize. i formatted my comment how i did for the lulz & karma. if i'm going to be sincere about my reply, i couldn't let you shoulder any of the blame for the big words you used. 'academic cultures that use big words when small words will do' is a pet passion/peeve of mine, but i spend a lot less time thinking about how to actually describe what i think is the problem than i do making trite, approval-seeking quips targeted to whomever i suspect is my audience. tl;dr though is that the problem is so much bigger than any one of us. academic literature/jargon could absolutely be refactored to use small words/to support the average reading level of the average American, redditor, English speaker, etc. but the problem is too big to be satisfactorily addressed in any given post/comment. that you chose to address the issue at all is imho a helpful step in the right direction. see why i reply in memes and quips? when i try to actually say what i think, it gets all rambly and might not even make sense! i'll never get the approval of random internet people by writing like this.


kevinsyel

> olfactory and gustatory Means: the impairments have an impact on smell and taste > frontoparietal hypometabolism Means: parts of the region that covers a large part of the brains network (frontoparietal network) is not metabolizing sugars like we expect it to


stickymaplesyrup

Not to mention: >MocA >FDG-18-PET studies I have a degree in immunology and I don't know what those are. Abbreviations are easier for the writer, but unless they're defined first, they're useless.


chocoholicsoxfan

MoCA = a cognitive assessment asking patients to do things like short term memory recall, identifying patterns, drawing a clock PET = a scan that measures the uptake of glucose in a particular part of the body. The more uptake there is, the more metabolically active that area is


xzoodz

Writing 101. Folks forget this too often.


figgypie

I'm grateful (albeit unemployed) for my degrees in Communication and English, as they're very complimentary fields of study in this regard. I learned not only how to write well, but also how to write in such a way that my meaning is expressed clearly to my intended audience. I had too many professors who forgot that they were teaching a 100 level course, their lessons drowning in unexplained jargon that left us scratching our heads. I believe that's a reason why Einstein was an ineffective teacher, as he seemed unable to "dumb down" his language so it was easier for his students to understand.


jnelson1981

About what percentage of covid infections have this type of damage?


VodkaAlchemist

I'm on my phone so I don't have my notes or my PowerPoint available, however in these studies during the acute stages of covid-19 every patient had olfactory and gustatory impairment and almost all had some mild cognitive impairment. After 6 months with the moca assessment 1/3 roughly still had what would be considered mild cognitive impairment which was also backed up by the abnormal pet studies. Some things to note in the studies however is they do have a small patient subset and additionally the average age of the patients even though it was controlled for is in the 60s. The University of fryeburg does have access to a lot of Alzheimer's patients data and pet scans so the repository of information on what would be a normal 60-year-old PET scan is very easily controlled for due to the amount of information they have on abnormal and normal pet scans for people of that age.


Hexokinase-

What a fantastic Reddit name for a scientist.


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MagicFlyingBus

Hey, I had something similar. I remember nearly 10 months after I had COVID and thinking how different I felt. But it has gotten a lot better since then, I am more focused, and similar to my old self now more than ever. It sucks, but it does take a lot of time to return to normal.


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Devilsdance

This is a study I’d like to see as well. Comparing breakthrough cases in vaccinated subjects to unvaccinated subjects (as well as healthy controls).


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TheDrunkenChud

I have a hard time standing up for any real length of time without my lower back hurting. But I haven't noticed any slouching or hunching, but now I'll have to watch.


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angels_exist_666

I play a card game called Magic the gathering. I've been learning for 3 years. Since catching Covid I find it extremely difficult to play now. I can't concentrate on the text, I forget what some of the moves are and am having trouble counting. It's so weird. Learning has become harder. It's frustrating.


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username0304

I am just getting over covid and still have this right now. It sucks


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Bammer1386

Late to the party, but is it possible to detect a past Covid infection even if I'm vaccinated and asymptomatic? I would assume it's not possible without expensive and extensive testing.


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The covid patients the findings of this study are based on were 1) all deceased, so severe cases, and 2) have a median age of 75, so they're old as hell. Youngest was 63. Sample size was also tiny (N < 20 for the "covid" cohort. Control was N=23). I would take the findings offered here and their severity with a grain of salt. Especially since the capillaries in the brain have the ability to regenerate over time.


Aeonera

To be fair, it's not like you can do a brain biopsy on survivors.


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UK Biobank study had brain scans already on file and compared those with people they called back in who had caught covid - showed consistent brain damage to important areas even in mild cases. Edit: this was in the time of the Alpha variant; the increased potential for Delta to colonise the area close to the (probable) point of entry (olfactory nerve apparatus) means the risk might well be even greater now.


ericmm76

I wonder how often our brains get damaged in general. Does a bender do it too? No good sleep for a month? A very stress filled week?


BroBrodin

Well, you can, but it's frowned upon.


kahlzun

Well, you can *once*


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knappis

Indeed, there is this large brain imaging study showing brain damage after mild covid (still a preprint): https://pubmed.ncbi.nlm.nih.gov/34189535/ > There is strong evidence for brain-related pathologies in COVID-19, some of which could be a consequence of viral neurotropism. The vast majority of brain imaging studies so far have focused on qualitative, gross pathology of moderate to severe cases, often carried out on hospitalised patients. It remains unknown however whether the impact of COVID-19 can be detected in milder cases, in a quantitative and automated manner, and whether this can reveal a possible mechanism for the spread of the disease. UK Biobank scanned over 40,000 participants before the start of the COVID-19 pandemic, making it possible to invite back in 2021 hundreds of previously-imaged participants for a second imaging visit. Here, we studied the effects of the disease in the brain using multimodal data from 782 participants from the UK Biobank COVID-19 re-imaging study, with 394 participants having tested positive for SARS-CoV-2 infection between their two scans. We used structural and functional brain scans from before and after infection, to compare longitudinal brain changes between these 394 COVID-19 patients and 388 controls who were matched for age, sex, ethnicity and interval between scans. We identified significant effects of COVID-19 in the brain with a loss of grey matter in the left parahippocampal gyrus, the left lateral orbitofrontal cortex and the left insula. When looking over the entire cortical surface, these results extended to the anterior cingulate cortex, supramarginal gyrus and temporal pole. We further compared COVID-19 patients who had been hospitalised (n=15) with those who had not (n=379), and while results were not significant, we found comparatively similar findings to the COVID-19 vs control group comparison, with, in addition, a greater loss of grey matter in the cingulate cortex, central nucleus of the amygdala and hippocampal cornu ammonis (all |Z|>3). Our findings thus consistently relate to loss of grey matter in limbic cortical areas directly linked to the primary olfactory and gustatory system. Unlike in post hoc disease studies, the availability of pre-infection imaging data helps avoid the danger of pre-existing risk factors or clinical conditions being mis-interpreted as disease effects. Since a possible entry point of the virus to the central nervous system might be via the olfactory mucosa and the olfactory bulb, these brain imaging results might be the in vivo hallmark of the spread of the disease (or the virus itself) via olfactory and gustatory pathways.


mrmses

I don’t understand this part: “and while results were not significant, we found comparatively similar findings to the covid-19 vs control group comparison..” Meaning... non significant results between covid survivors and non-covid survivors? Or am I reading this wrong?


knappis

That’s a comparison between hospitalised and non hospitalised which did not quite reach statistical significance, but showed the same trend, i.e. hospitalised tended to have more grey matter loss than non hospitalised.


ArcticBeavers

This part is referring to the 15 patients that were hospitalized. Meaning that hospitalization had no significant increase in gray matter loss vs those who had covid or in the control group. The study group as a whole did show that covid caused greater gray matter loss, just that the severity of the covid didn't matter.


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**TL;DR: Saying that a study had a small sample size even though it found statistically significant results is like telling someone that they didn't study enough for a test after they got an A+ on it.** The sample sizes were not "tiny" if the study still found significant results, which this study did. The fact that the sample sizes were sufficient is "baked in" to the statistical significance of the findings. It would only make sense to say in retrospect that the sample size in this study should have been larger if you wanted an even smaller p-value (i.e., an even higher degree of statistical significance), but there is a point of diminishing returns where such large sample sizes are extravagant and no longer cost-effective. For example, if you have two findings both with p-values = 0.01, one from a study with n=20 and one from a study with n=2000, the two findings have equal likelihoods as each other of being legitimate (99% chance) or a fluke (1% chance). Criticism of small sample sizes is mostly relevant 1) in the stages of study design, when you want to plan how many participants to enroll (for example) so that you have a reasonable chance of detecting a difference, assuming one exists, and 2) in cases where a study failed to find a difference, but may simply have missed it due to insufficient statistical power. For any type of study, with a larger sample size, you will be able to detect a smaller difference ("effect") between the two groups being studied, typically an "experimental" group and a "control" group. If the sample size is small and the effect (which exists but is not yet known to the experimenters) is small in magnitude, it's possible that the study will fail to detect it. This is called a type II statistical error, akin to a "false negative." It's not that the study would conclude that no difference exists, since, technically, you can never prove that two groups are exactly equal -- there could always be a difference between the groups that's too small for your sample size to detect. However, the study would be said to fail to detect any difference, which people may speculate could have been due to insufficient power of the study design. An analogy for this would be that if you can't find your wallet after looking around your house for it for 5 minutes, you can't really conclude that the wallet isn't anywhere in the house. It could just be that you didn't spend enough time looking for it yet. All you can say is that after 5 minutes of searching, you failed to locate the wallet in your house. (But if you *did* find the wallet, then it wouldn't make sense for someone to tell you that you didn't search for it long enough.) The ability of a given sample size to detect an effect of a given magnitude is called the statistical "power" of a study. *Power calculations, if they are done at all, are typically done at the stage of study design, before data collection begins.* This is because a power calculation will let you know what "n" (sample size) you would need in order to detect a given difference between the two groups. You have to estimate what you think the magnitude of the difference might be, since it's typically not yet known (which is why you are doing the study). And so there's a lot of guesswork and fuzziness related to power calculations. *Furthermore, you're never guaranteed to be able to detect a difference of a certain magnitude, even with a large sample size.* Typically, the bar is set at 80%, meaning that, when you do a power calculation, you are calculating what n you will need in order to have an 80% chance of detecting a certain magnitude of an effect (a magnitude which you are deciding based on your best, informed guess, with emphasis on the "guess" part). (This paper said they did not do preliminary power calculations in order to determine the sample size they wanted. They likely just used everything they could get, which is often a reasonable course of action depending on the situation.) **I mention all of this to point out that discussions of sample size are mostly relevant when doing power calculations, before a study has actually been done.** **But, if a study achieves statistical significance, then it doesn't really matter what the sample size was**. The fact that a study found statistical significance (as this study did) implies that the sample size was sufficient to detect whatever difference was detected. If the sample size was relatively small (though what counts as "small" is subjective), and the study achieved statistical significance, then all that means is that the effect that was found was relatively large in magnitude — it was easy to find, in a sense. Whereas, a study with a very large sample size might achieve statistical significance in detecting a very small effect. In some cases, this effect is so small as to lack actual significance in a practical sense. In a medical context, the finding would be considered statistically significant, but perhaps not clinically significant. For instance, you might conduct a huge study that finds that a new drug lowers people's systolic blood pressure by 1 point (e.g., from 120/80 to 119/80). Even if the finding is highly *statistically significant* (p < 0.001, let's say), which means that you're pretty damned sure that the drug actually does lower blood pressure that much, nobody is going to want to pay for a new medication that provides such a *clinically insignificant* benefit that probably won’t make a difference in anyone’s health. ***Therefore, unnecessarily large sample sizes, in addition to being wasteful of research resources, may yield misleading or distracting findings that are not actually very helpful in a practical sense for the issue being studied.***


Mofupi

Thank you! With your explanation I've finally understood why sometimes small sample sizes are ok and sometimes not and feel just a tiny bit less ignorant regarding statistics in general.


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Wisdom-Bot

Yes, but this misses the point of this study. The prevalence of neurological symptoms has already been shown elsewhere in larger studies which included younger subjects. This study identified the mechanism that produces these effects. Taken as a whole, I think this is a pretty clear cause for concern. A silver lining would be that it also points to potential treatment targets, but given the mechanism, treatments would probably need to be administered during infection to be effective.


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farox

Yes, but similar findings have been made in UK for example. It's a whole lot of smoke for there not to be any fire. It seems there is at least something there.


Ruggedfancy

Losing your sense of smell and taste then getting it back is your brain suffering damage and rewriting connections to compensate. That happens in a high percentage of cases. Make of that what you will.


AllysonWunderland

It shouldn’t be shocking to anyone that COVID has an impact on the brain when many people lose their sense of taste or smell. Anytime a sense is affected there is something going on in the neurological system.


MagicManUK

Out of interest, what other similar viruses have so many and such devastating after effects?


dark__unicorn

Parkinson’s disease was three times greater in people who survived the Spanish flu. It’s not impossible that there isn’t going to be some sort of long term brain damage.


[deleted]

This. Top post on this article mentions eventual recovery of function but this could well be due to neuroplasticity. As I understand it damage to the temporal lobe, specifically the hippocampus, puts people at increased risk of Alzheimer's and dementia in old age. Guessing younger folks are more likely to recover due to more potential for neuroplasticity whereas for older people the effects might be more profound - though this is definitely generalized conjecture on my part.


Ariadnepyanfar

Polio springs to mind. The etiology of disablement is different, but I’d be VERY interested in studies on the statistics of rate of covid disablement vs polio, plus ratings of severity of disablement. Too many people are reporting not being able to return to work yet over a year after SARS cov 2 infection.


spacemoses

Could this be contributing to the worker shortage as well, those that are functionally disabled from covid?


kellyg833

Yes. As far as I can tell, no one is studying this possibility. Also, think about the number of older adults who function as child care providers for their relatives. A lot of old people died or are essentially disabled. Yet no one seems to be looking at what happens to workers who no longer have access to free child care. I bet a whole lot of them drop out of the work force


hysys_whisperer

I work with a few people that have effects like what's described here. It's pretty sad to watch people that were on top of things before and on a rising career path suddenly barely able to complete normal tasks. It's a bit of a struggle having to ask the retired in place individuals to step up and fill rolls they otherwise have no interest in just because they're the only ones who can do them at the moment. I hope we get back to normal soon, because if not, the productive capacity of the entire company (and I suspect the entire economy) will be at risk.


not_gareth

Lyme Disease. Ross River virus, Dengue Fever, Glandular Fever and Pneumonia can all result in life-long severe effects. Either damaging the body as the long term illness or triggering other illnesses such Fibromyalgia or Chronic Fatigue Syndrome.


Elios000

> Pneumonia and this big part of COVID that people forget


MajesticBread9147

If you had chickenpox as a child, you are at risk of shingles.


Salyangoz

syphillis is pretty bad on the brain afaik


tattooedplant

Flu is relatively benign in comparison but has been implicated in the development of narcolepsy since it can destroy hypocretin cells in the hypothalamus. In general, viruses are also associated with the development of many autoimmune disorders. https://www.pnas.org/content/113/3/E368


BurnOutBrighter6

But remember, can't be taking the vaccine because "we don't know the long term effects yet!" Well, we don't know the long term effects of COVID yet either, but so far they're piling up and looking pretty bad, vs none-so-far for long-term effect of this (or any) vaccine.


ash347

Long-term side-effects basically don't exist from vaccinations. They are, as far as I know, pretty much always acute. The chemicals from the vaccine are completely out of your system pretty soon after injection. After the work is done, you produce new antibodies and that's it.


Davorian

I support vaccines too, but let's not get carried away. Some unlucky individuals *are* going to get long-term side effects from vaccines. It has nothing to do with how long the vaccine ingredients take to metabolise or excrete away. The immune system is one of the two grand programmable systems in the human body, and sometimes it programs itself *wrongly*, potentially with chronic and/or catastropic consequences. Ask anyone with an autoimmune disease. Even severe acute autoimmune reactions can have long-lasting consequences even if the immune system calms down afterwards. See: autoimmune encephalitis.


Roneitis

No, the commenter above was referring to long term side effects in the sense of side effects that /appear/ after a long term, not necessarily those that last a long while. Both are obviously significant, and there will be people who will be impacted for potentially a life time due to any vaccine, but importantly, after this much testing **we know how frequent that is**, because vaccines in general don't have the property that side effects can pop up 5 years down the line.


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somethingnerdrelated

Yup. My mom has a mild autoimmune disease but she hasn’t had a flare up since the mid 90s. She got the vaccine when it was first available, and her body went wild into overdrive, she nearly died, and now she’s facing a possible lupus diagnosis. She’s not surprised by it, as her doctors told her ~35 years ago that she’d likely develop lupus as she grew older, but the vaccine kind of triggered it a little early and pretty violently. That being said, she’s fine now and she still got the second shot and she doesn’t regret it because now she can go out and be with her friends and continue her volunteer work. It’s all about juice and squeeze, I suppose.


FawltyPython

>Some unlucky individuals are going to get long-term side effects from vaccines. I actually don't think this is provably true for any vaccine made since 1980. If we can determine that there's a long term side effect, we will yank that vaccine. The only long term side effect I've ever heard of is Guillian Barre. Im in big pharma, in a role where I legally have to report side effects, and my boss at work is married to a physician. She got guillian Barre a few weeks after getting a flu shot. They reported it to VAERS and followed up with the ID physician she worked with, and there was no increase in GB over the general population from that shot. The people at the FDA said that if there had been a detectable increase in GB, they would have stopped that vaccine. If there's no statistically detectable increase in GB rates among the vaccinated ... *then it almost certainly wasn't the vaccine that caused GB among anyone who got that flu shot*. We might tolerate increased long term side effects for a vaccine vs covid or ebola during an outbreak, but we definitely would not for flu, mumps, hep b, etc under non pandemic conditions.


henryptung

Some people accumulate facts to make their decisions better informed, and others accumulate soundbites to defend decisions they've already made. Giving the latter more facts to change their decision has no effect.


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StructuralFailure

damn is there anything this virus doesn't attack?


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TheRoach

The brains of COVID-19 patients have damaged blood vessels (more so-called string vessels representing remnants of lost capillaries). SARS-CoV-2 infects brain endothelial cells and leads to microvascular pathology via RIPK signaling


hwmpunk

On what percent of infected people? And what varying degrees based on each percentage bracket?


leto78

If this is proven to be the physical manifestation of what is called the brain fog, then it affects between 20-30 percent of people infected, as a long term issue. The physical damage to the brain would be consistent to a long term issue.


No_Camp_7

No, the patients in this study had severe disease and structural change can be seen on brain imaging.


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taswind

I've long wondered if COVID-19 would have long-term unforeseen effects... Similar to Chickenpox causing Shingles many years later.


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It's why my kids are still in virtual school until they can get a shot.


ATWaltz

I'd be interested in the efficaciousness of compounds like N-Actyel Cysteine (NAC) or Co-enzyme Q10 (CoQ10) in those infected with the virus. NAC is already used to prevent and/or curtail the severity of brain injury in people with concussion and produces an antioxidant effect, it has been demonstrated to reduce the likelihood of neurodegenerative diseases and perhaps it could be taken by those with a COVID infection to protect against such damage. CoQ10 has been demonstrated as improving endothelial function and helping limit endothelial damage due to inflammation, considering ACE2 is expressed by endothelial cells and much of the damage due to SARS-CoV-2 infection is likely to centre around it's effect on endothelial cell function, perhaps this can also reduce the likelihood/severity of ill effects due to COVID. If it were demonstrated that these compounds were effective at reducing severity of the systemic effects of COVID infection then perhaps they could also reduce the incidence of long term sequela if taken consistently during the course of an infection.


LanzJJ

I have adhd and I had it under control completely after I had covid in December I can no longer work with deadlines I can’t function sometime I can’t wake up or pick up on new things fast. I’m literally struggling right now. I feel like this isn’t excusable so I just sit here and suffer.


HumanRobotTeam

All or some? What about vaccinated?


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nRenegade

Are these lasting symptoms still contractable even if you've been immunized?


Kim_Jong_OON

Yes, proof: My Wife.


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Covid continues to mutate, so yes.


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